Sqstm1 siRNA_Lentivectors
- Known as:
- Sqstm1 siRNA_Lentivectors
- Catalog number:
- i064839d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Sqstm1 siRNA_Lentivectors
Related genes to: Sqstm1 siRNA_Lentivectors
- Gene:
- SQSTM1 NIH gene
- Name:
- sequestosome 1
- Previous symbol:
- PDB3, OSIL
- Synonyms:
- p62, p60, p62B, A170
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-13
- Date modifiied:
- 2019-03-07
Related products to: Sqstm1 siRNA_Lentivectors
Related articles to: Sqstm1 siRNA_Lentivectors
- Autophagy is critical for cellular homeostasis and may participate in the pathogenesis of pulpitis, although its underlying mechanisms remain unclear. This study investigated hypoxia-induced autophagy in human dental pulp cells (HDPCs) and its molecular basis. - Source: PubMed
Publication date: 2026/06/15
Wang XiaoheZhang YangyangWu ZeyuMa LiLian BingjieZhao Jin - Arterial hypertension is a socially significant disease, one of whose complications is cerebral ischemia. Various mechanisms are involved in the adaptation of neurons to hypoxia, including those modulating mitochondrial activity, the autophagy system, and the regulation of apoptosis. - Source: PubMed
Sukhorukov V SBaranich T IAnufriev P LVelts O VVoronkov D NRyabova M SLazarev D SEgorova A VCharyeva I GYatskovskiy A NGlinkina V V - Juvenile neuronal lipofuscinosis (JNCL) is a rare disease caused by mutations in the CLN3 gene. It leads to early vision loss mediated by retinal degeneration. Impaired autophagosomal-lysosomal degradation is a major hallmark of JNCL pathology, and neuroinflammation has also been postulated to play a role in its pathogenesis. Thapsigargin, a selective inhibitor of sarco/endoplasmic reticulum Ca-ATPase, inhibits autophagy, leading to an accumulation of autophagosomes/autophagophores in cells. Cells with defective CLN3 protein function have been found to be particularly sensitive to the anti-autophagic effects of thapsigargin. Here, we characterized the effects of thapsigargin on inflammatory cytokines and autophagic markers in ARPE-19 cells using ELISA and western blotting. We further examined these effects in cells deficient in CLN3 function by exposing the cells to CLN3 siRNA and testing whether the effects of thapsigargin could be modulated by the well-known autophagy activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR). Thapsigargin induced the accumulation of LC3 and p62/SQSTM1, consistent with impaired autophagic flux in ARPE-19 cells. Additionally, we observed that thapsigargin possessed pro-inflammatory potential, as it induced the release of IL-6 in ARPE-19 cells, no inflammasome activation was detected. Both effects were enhanced by CLN3 siRNA and alleviated by AICAR. In conclusion, thapsigargin-induced impaired autophagic flux and the accompanying inflammatory response are more pronounced in CLN3-deficient ARPE-19 cells, indicating that loss of CLN3 function affects both autophagy and inflammatory signaling. - Source: PubMed
Publication date: 2026/06/16
Torsti TommiHytti MariaToppila MaijaForsberg Markus MKauppinen Anu - Oncogenic condensates act as biophysical sanctuaries that stabilize malignant survival programs. However, a universal regulator capable of orchestrating the integrated biophysical axes governing cellular phase behavior has remained elusive. Here, we introduce a sovereign singularity framework, presenting a deductive biophysical model that positions the indoleamine melatonin as a master regulator of biological phase separation. A systematic synthesis and integrative bioinformatics analysis were performed to identify the intersection between melatonin-responsive genes and the phase-separation proteome. We identified a core 26-gene regulatory signature-including AR, BCL2, CGAS, CTNNB1, EP300, EZH2, EGFR, IKBKG (NEMO), KEAP1, KDM1A (LSD1), LEF1, MYC, NANOG, PRNP (PRP), SMAD3, SOX9, SQSTM1, TFEB, TFAM, TP53, TWIST1, USP10, WWTR1 (TAZ), VIM, YAP1, and YTHDF3-at the intersection of melatonin signaling and condensate architecture. We propose that melatonin utilizes a tri-lever framework of redox tuning (Lever I), multivalent plasticization (Lever II), and dielectric recalibration (Lever III) to render oncogenic programs biophysically untenable. This model provides a mechanical basis for high-resolution regulatory outcomes that modulate the organizational logic of nuclear decision-making (Axis I), state-transition (Axis II), and stress-adaptation (Axis III) condensates. Our results define a strategic platform for disrupting condensate-driven malignancy through the systemic modulation of the cellular biophysical landscape. - Source: PubMed
Loh DorisChuffa Luiz Gustavo de AlmeidaSeiva Fábio Rodrigues FerreiraReiter Russel J - Abdominal aortic aneurysm (AAA) remains a life-threatening vascular disease without effective pharmacologic therapy. Although 3-hydroxyanthranilic acid (3HAA), a kynurenine-pathway metabolite with dual redox effects, has been implicated in vascular diseases. How 3HAA instigates AAA is poorly defined. - Source: PubMed
Publication date: 2026/06/12
Ramprasath TharmarajanHan Young-MinDing YeCarr Sean MichaelZou Ming-Hui